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The co-evolution of humans and microbes that colonise the GI tract is shaped by environmental factors and evolved to promote health.1 Microbial derangements (termed dysbiosis) have been observed for a variety of intestinal and extraintestinal diseases.1 Metabolic, autoimmune, liver and intestinal disorders have been linked to microbial dysbiosis which promotes susceptibility to inflammatory disease in some cases as largely assessed in animal models.2 Intestinal dysbiosis has also been implicated in colorectal cancer3 and microbes may determine treatment response for non-intestinal malignancies.4

For more than 10 years, intestinal microbial alterations have been associated with localised radiation in humans and mouse models.5–8 Importantly, mice that lack colonisation of microbes (ie, raised germ free) were resistant to lethal radiation enteritis, indicating that the microbiota controls intestinal disease processes consequent to radiation-induced damage.9 In this...]]>

2017-12-12T01:55:36-08:00info:doi/10.1136/gutjnl-2017-314279hwp:master-id:gutjnl;gutjnl-2017-314279BMJ Publishing Group2018-01-01Commentary67112http://gut.bmj.com/cgi/content/short/67/1/2?rss=1
The incidence of pancreatic ductal adenocarcinoma (PDAC) is increasing. The projection that it will surpass breast cancer to become the second-leading cause of cancer-related deaths by 2030 serves as a wake-up call to stakeholders, including healthcare systems and researchers.1 Earlier diagnosis is one factor that could alter this trajectory. Correspondingly, the research community has made substantial efforts to find biomarkers that will enable the diagnosis of pancreatic cancer at a stage where it can be successfully treated.2 There are however, significant challenges. Pancreatic cancer is a very heterogeneous disease with great interindividual variation, as well as significant heterogeneity within the tumours of individuals.3 4 This calls for large sample sizes to ensure adequate representation of subtypes. Moreover, biomarker development programmes require samples to be separated into independent training and test sets, further increasing the quantity of samples needed. However, the number...]]>2017-12-12T01:55:36-08:00info:doi/10.1136/gutjnl-2016-313665hwp:master-id:gutjnl;gutjnl-2016-313665BMJ Publishing Group2018-01-01Commentary67123http://gut.bmj.com/cgi/content/short/67/1/3?rss=1
Humans and viruses have coevolved over thousands of years; however, very few viruses are able to manifest as chronic infections with most being cleared after an acute course. Consequently, success of the human species has relied on a functional immune system that is capable of fighting off most viral pathogens. The heptatitis B virus (HBV) is one of the most successful viruses to establish chronic infection in man with over 300 million individuals currently infected worldwide and over 2 billion humans having been infected by this virus.1 These numbers underscore the tremendous ability of HBV to thwart the human immune system and establish chronic infection. In this issue of Gut, Lim et al2 have provided evidence for a new mechanism through which HBV is able to establish and maintain chronic infection.

They specifically examine the role of the enigmatic HBx protein3 in the regulation...]]>